Abstract
RAS-related C3 botulinum toxin substrate 1 (Rac.1) is one of the important members of Rho GTPases. It is well known that Rac1 is a cytoskeleton regulation protein that regulates cell adhesion, morphology, and movement. Rac1 is highly expressed in different types of tumors, which is related to poor prognosis. Studies have shown that Rac1 not only participates in the tumor cell cycle, apoptosis, proliferation, invasion, migration and angiogenesis, but also participates in the regulation of tumor stem cell, thus promoting the occurrence of tumors. Rac1 also plays a key role in anti-tumor therapy and participates in immune escape mediated by the tumor microenvironment. In addition, the good prospects of Rac1 inhibitors in cancer prevention and treatment are exciting. Therefore, Rac1 is considered as a potential target for the prevention and treatment of cancer. The necessity and importance of Rac1 are obvious, but it still needs further study.
Highlights
The classical Rho-GTPase family consists of RhoA (RhoA-RhoC), Rac (Rac1-Rac3 and RhoG), Cdc42 (Cdc42, RhoJ, and RhoQ), and RhoF (RhoD and RhoF) [1]
Knocking down PKC-can lead to a decrease in the proliferation and metastasis of colorectal cancer (CRC) cells because protein kinase C-z (PKC-z) reduces the nuclear translocation of b-Catenin and affects the Rac1-PAK1-b-catenin signaling cascade [39]
We have further found that diallyl disulfide (DADS) inhibits the migration and invasion of colorectal cancer cell line SW480 by regulating the Rac1-ROCK1/PAK1-LIM kinase1 (LIMK1)-ADF/cofilin signaling pathway [104, 105]
Summary
The classical Rho-GTPase family consists of RhoA (RhoA-RhoC), Rac (Rac1-Rac and RhoG), Cdc (Cdc, RhoJ, and RhoQ), and RhoF (RhoD and RhoF) [1]. The Rho-GTPase family (Rho, Rac and Cdc42) plays an important role as cytoskeleton regulatory proteins [13], which is best confirmed in fibroblasts and can be observed in many other cell types, such as epithelial cells, endothelial cells, astrocytes and mast cells [14,15,16]. Actin polymerization regulated by Rac and Cdc can promote cell movement, leading to migration and invasion [19]. When FER is knocked out, the Rac1-PAK1 signaling pathway is inactivated and the migration ability of ovarian cancer cell CAOV4 decreased [38]. Knocking down PKC-can lead to a decrease in the proliferation and metastasis of colorectal cancer (CRC) cells because PKC-z reduces the nuclear translocation of b-Catenin and affects the Rac1-PAK1-b-catenin signaling cascade [39].
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